|Year : 2016 | Volume
| Issue : 1 | Page : 23-28
Ventricular septal defect from blunt cardiac injury: A case report and meta-analysis of 64 patients from 61 reviews
Jonathan Nwiloh1, Obinna Orakwe2, Kenneth Etukokwu2, Uzoma Okechukwu2, Norbeth Iziga2, Chinyere Onyenwuzor2
1 Atlanta Medical Center, Atlanta, GA, Nigeria
2 Dr. Joe Nwiloh Heart Center, St. Joseph's Hospital, Adazi-Nnukwu, Anambra State, Nigeria
|Date of Web Publication||25-Jul-2016|
Dr. Joe Nwiloh Heart Center, St. Joseph's Hospital,Adazi Nnukwu, Anambra State
Source of Support: None, Conflict of Interest: None
A 36-year-old male motorcyclist involved in a motor vehicle accident (MVA) with loss of consciousness and sustained multiple orthopedic injuries and a traumatic ventricular septal defect (VSD) which was hemodynamically stable. He then underwent emergency orthopedic surgery and was discharged after 5 weeks to rehabilitation. Subsequently, 6 months later, he underwent an elective repair of a 1.5 cm apical septal defect with uneventful recovery. A meta-analysis of 61 other reports of traumatic VSD revealed MVA as the most common etiology in 57.8%, predominantly males in 85.5% and younger age group <30 years in 87.5%. The midmuscular septum was involved in 43.6%, and patch closure was used in the majority of patients performed through a right or left ventriculotomy. Operative mortality was zero with elective versus 27.3% for emergency repairs, which also had a 27.3% VSD recurrence. 28.6% of the patients required concomitant cardiac surgical procedures while two patients (4.1%) both with perimembranous VSD required a permanent pacemaker. Less invasive transcatheter closure was successfully deployed in three patients without any complications, and it is an alternative in patients with a suitable anatomy and no associated cardiac injuries requiring surgery. Conservative therapy as a mainstay of treatment should be reserved for asymptomatic small defects with hemodynamically insignificant shunts.
Keywords: Motor vehicle accident, septal defect, trauma
|How to cite this article:|
Nwiloh J, Orakwe O, Etukokwu K, Okechukwu U, Iziga N, Onyenwuzor C. Ventricular septal defect from blunt cardiac injury: A case report and meta-analysis of 64 patients from 61 reviews. Niger J Cardiovasc Thorac Surg 2016;1:23-8
|How to cite this URL:|
Nwiloh J, Orakwe O, Etukokwu K, Okechukwu U, Iziga N, Onyenwuzor C. Ventricular septal defect from blunt cardiac injury: A case report and meta-analysis of 64 patients from 61 reviews. Niger J Cardiovasc Thorac Surg [serial online] 2016 [cited 2020 Dec 3];1:23-8. Available from: http://www.nigjourcvtsurg.org/text.asp?2016/1/1/23/186851
| Introduction|| |
Traumatic ventricular septal defect (VSD) from blunt cardiac injury (BCI) is rare with <100 cases, and mostly of single case report in the English literature since the 1950s. Considering the high incidence of high-speed motor vehicle accidents (MVAs) and the relatively few reported cases of traumatic VSD, it is likely that either most are fatal and do not survive to reach the hospital or they are small and go undiagnosed. Increased awareness and heightened suspicion among health-care providers treating BCI patients involved in a high-speed MVA presenting with systolic heart murmur, cardiac contusion with acute electrocardiogram (EKG) changes, and elevated cardiac enzymes should prompt further investigative workup including a transthoracic echocardiogram (TTE) to rule out structural heart damage.
| Case Report|| |
A 36-year-old male motorcyclist was hit by a sports utility vehicle, sustaining loss of consciousness and multiple injuries including open left femur and tibia, closed right and left wrists' fractures, and pulmonary contusion. On presentation to the emergency room, Glasgow coma score was 15, blood pressure was 138/58 mmHg, pulse was 112/minute, respiratory rate was 18/minute, and oxygen saturation was 99% on room air. Significant physical findings were the left thigh deformity with nonpalpable pedal pulses but audible by Doppler, ankle brachial index of 0.6, and audible heart sounds with a grade 4/6 pan systolic murmur. EKG showed the right bundle branch block and inferior wall myocardial infarction [Figure 1]. Cardiac enzyme creatine kinase was 1831 (normal: 49-397 IU/L), CKMB was 239.7 (normal: 0.60-6.30 ng/ml) 13.1%, troponin I was 91.95 (normal <0.50 ng/ml), and brain natriuretic peptide was 79.4 (normal <100.00 pg/ml). TTE revealed an apical VSD with the left-to-right shunt and ejection fraction of 50-60%. The patient's mother denied any history of congenital heart disease or any other known prior cardiac disease. The patient then underwent emergency orthopedic surgery after cardiology clearance, and subsequently 2 days later, a right heart catheterization which showed oxygen step up at the right ventricular level with right atrium (RA), right ventricle (RV), and pulmonary artery (PA) oxygen saturations of 63%, 83%, and 80%, respectively, and Qp/Qs 2.0. Pressures were RA 12, RV 54/7, 16, and PA 58/17,35. The left heart catheterization showed normal coronaries, apical VSD, and preserved left ventricular systolic function. Since there were no significant cardiac symptoms, he was treated conservatively and discharged to a rehabilitation center after 5 weeks hospitalization with instructions to follow-up as outpatient. Over the following months, he developed symptoms of heart failure with worsening shortness of breath, palpitations, orthopnea, and paroxysmal nocturnal dyspnea. Pertinent physical findings were prominent apical pulse, grade 4/6 systolic murmur, and mild finger clubbing. Repeat TTE showed persistent VSD with the left-to-right shunting, confirmed on cardiac magnetic resonance imaging (MRI) [Figure 2]. Six months after his accident, he then underwent elective surgery via a median sternotomy and cardiopulmonary bypass under mild hypothermia and cold blood cardioplegic cardiac arrest. Through a left ventriculotomy, a 1.5 cm apical VSD with fibrous edges was closed with a hemashield patch using 2/0 Ethibond with pledgets [Figure 3]a and b. Oxygen saturations postcardiopulmonary bypass were RA 81%, RV 83%, PA 80%, and ascending aorta 100%. Intraoperative transesophageal echocardiogram (TEE) showed no residual VSD or shunting. The postoperative course was uneventful, and he was discharged home on the 4 th postoperative day. The patient is almost on 4-year postsurgical repair and continues to do well with no residual VSD or cardiac symptoms.
|Figure 2: Cardiac magnetic resonance imaging with arrow pointing to the ventricular septal defect.|
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|Figure 3: (a) Repairing ventricular septal defect. (b) Completed patch repair of ventricular septal defect.|
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| Discussion|| |
The spectrum of BCI presentation ranges from the absence of clinical manifestations, arrhythmias to rupture of cardiac structural components. BCI has been estimated to occur in 20% of all blunt thoracic trauma patients and up to 76% in those with severe thoracic injury or multiple injuries. BCI also accounts for about 20% of all MVA fatalities. , VSD which is part of the spectrum of BCI is surprisingly relatively rarely diagnosed clinically in spite of the high incidence of MVA in the USA. VSD has been estimated to occur in 2-10% of survivors of multiple blunt trauma.  However, Parmley et al.  in a 1958 review identified only five patients with isolated VSD out of 5467 cases with blunt chest trauma. This suggests that perhaps VSD is underdiagnosed or missed because most are likely small and hemodynamically insignificant, and may close spontaneously over time without any clinical manifestations. The larger defects with significant left-to-right shunting are, however, more likely to become symptomatic and to be either diagnosed at the time of initial injury or subsequently after the onset of cardiac symptoms. Although all ages and gender are involved in MVA, the majority of reported VSD from blunt trauma in the literature are predominantly children and young adults and mostly males. In a meta-analysis of 61 reviews ,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,, in the English literature from 1958 to 2015 comprising 64 patients, the mean age was 19. 25 ± 11.90, ranging 3-60 years [Table 1]. There were 53 (85.5%) males, 9 (14.5%) females, and 2 with unknown gender. Sixteen (25.0%) patients were <10 years, 34 (53.1%) were <20 years, and 56 (87.5%) were <30 years, with only 4 (6.25%) older than 40 years of age. MVA was the most common etiology accounting for 58.7%, and among those with stated location, the midmuscular septum was the most frequent site in 43.6% of the patients [Table 2]. Two patients had previous mitral valve replacement, one 24-year-old male with ATS and a 48-year-old female with St. Jude 1 year and 9 months, respectively, prior to their MVA. The male required emergency surgery with patch closure of an apical VSD, whereas the female had elective surgery 11 months later with patch closure of perimembranous VSD and tricuspid valve repair, both doing well from the surgery. In reports stipulating surgical approach to repair, the right ventriculotomy was most frequently used in 36.4% (12/33) followed by the left ventriculotomy in 27.3% of the patients (9/33). Patch closure was utilized in 67.3% (33/49) and concomitant cardiac procedures were required in 28.6% of the patients (14/49) [Table 3]. 22.4% (11/49) of the patients including 2 requiring preoperative intra-aortic balloon pump were operated emergently with 27.3% (3/11) mortality. There was zero mortality in the 38 (77.6%) patients undergoing elective surgery. Overall, postoperative residual VSD was present in 14.2% of the patients (7/49). However, in the emergency group, the incidence of residual VSDs was 27.3% (3/11), and all the three required re-operation at 6 weeks, 2 months, and 10 months postoperatively. One of these reports stated that the VSD size as 4 cm, one simply large and the third had no mention of defect size, but they were all located in the midmuscular septum and closed with a patch. Residual VSD in the elective group was 10.5% (4/38), 2 apical, 1 muscular, and 1 perimembranous without the mention of defect sizes in any. However, 3 had patch and 1 primary closure. All the four residual defects were considered small and hemodynamically insignificant and one had closed by 2 months after surgery. Complete heart block requiring permanent pacemaker occurred in 4.1% of the patients (2/49), both with perimembranous VSD closed with a patch. One patient had emergency surgery with severe tricuspid regurgitation from torn chords and died postoperatively, while the second patient had elective surgery and did well postoperatively. Three patients, two with apical VSD, one site not stated, and defect size undocumented underwent successful transcutaneous closure without any complications. In the 11 patients treated conservatively, mortality was 27.3% (3/11) and included the two patients who refused surgery and one patient in Nigeria with no local surgical expertise available. Although all age groups are involved in MVA, almost all patients reported in the literature with traumatic VSD following deceleration type injuries are either children or young adults, with the injury rarely seen in middle-aged patients above the age of 40 years. The explanation for this age disparity is unclear. VSD following BCI has been postulated to involve 3 possible mechanisms enumerated below: (1) Excessive intracardiac pressures from acute compression of the heart between the sternum and the spine during late diastole with the valves closed and ventricles filled with blood (isovolumetric systole). , (2) Myocardial injury causing microvascular disruption with consequent infarction and liquefaction of the septum.  (3) Possible reopening of a healed and weakened congenital septal defect from deceleration injuries. 
To explain the apparent rarity in middle-aged and older adults, we speculate two possible theories that relate to the first mechanism for traumatic VSD described above. The thinner and less hypertrophic heart of most children and young adults may be more prone to rupture from the additive sudden high intraventricular pressure generated by deceleration forces of the heart been struck between the sternum and spine when it occurs during the isovolumetric phase of the cardiac cycle. Second, the trivial-to-mild mitral and tricuspid regurgitation seen with aging in many adults may possibly provide a pop off decompression of the intraventricular forces generated during deceleration injuries to prevent septal rupture seen in the younger age groups. It is also plausible that most adults with VSD from BCI do not survive to the hospital for antemortem diagnosis, or that small hemodynamically insignificant defects in thickened hypertrophic septum may go undiagnosed. Depending on the pathophysiology of the VSD, it might be diagnosed at initial presentation as in our patient or develop later as reported in some of the other series. Due to the relative rarity of VSD despite the high volumes of MVAs worldwide, no single institution has accumulated enough experience to report any significant numbers. Therefore, based on our meta-analysis of 64 patients, we make the following observations and recommendations.
- MVA is the most common etiology, and defects occur mostly in the midmuscular septum
- Children and young adults <30 years appear more susceptible to VSD after BCI and account for about 87.5% of the reported cases, and they should undergo closer scrutiny when seen in the emergency room in the setting of significant BCI
- Majority of the hemodynamically significant VSDs with left-to-right shunts can tolerate initial conservative management followed either by elective surgery in 8-12 weeks depending on the symptoms or transcatheter closure when the anatomy is suitable, and there are no other associated cardiac injuries requiring surgery
- Emergency surgery when required due to hemodynamic instability refractory to standard medical treatment carries a high operative mortality and recurrent VSD rate
- Patch closure either through a right or left ventriculotomy is preferred for most defects except perimembranous or subinfundibular VSD, when transtrial is preferable
- Concomitant cardiac procedures may be required in almost a third (28.6%) and permanent pacemaker in 4.1% of the patients after surgical repairs.
| Conclusion|| |
A high index of suspicion is required in BCI patients presenting with a systolic murmur, abnormal EKG, or elevated cardiac enzymes. TTE should be performed as a screening tool if structural heart disease is suspected and repeated after a few days if murmur persists and no abnormalities identified at the initial screening echocardiogram. If the index of suspicion remains high with an equivocal or normal study, other diagnostic tools include MRI and cardiac catheterization to confirm VSD and quantify the severity of shunt.
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[Figure 1], [Figure 2], [Figure 3]
[Table 1], [Table 2], [Table 3]